Seizures in cats are caused by various onsets. Cats can have reactive, primary (idiopathic) or secondary seizures. Idiopathic seizures are not as common in cats as in dogs however a recent study conducted showed that of 91 feline seizures, 25% were suspected to have idiopathic epilepsy. In the same group of 91 cats, 50% were secondary seizures and 20% reactive.

Idiopathic epilepsy does not have a classification due to the fact there are no known causes of these seizures, however both reactive and symptomatic secondary epilepsy can be placed into classifications.

Benign neonatal seizures include two disorders benign idiopathic neonatal seizures and benign familial neonatal seizures. They are not classified as epilepsy. Anticonvulsants are not needed. And those affected do not develop epilepsy when they grow up.

Like many other types of seizures, gelastic seizures are hard to control for an extended period of time. The best outlook is for children suffering the seizures due to a benign tumor in their hypothalamus. The removal of these tumors can be effective not only for the frequency of the seizures, but also the behavioral and cognitive symptoms that come along with the syndrome. Cases have also been described where that antiepileptic drugs have stopped seizures fully.

The prognosis for Rolandic seizures is invariably excellent, with probably less than 2% risk of developing absence seizures and less often GTCS in adult life.

Remission usually occurs within 2–4 years from onset and before the age of 16 years. The total number of seizures is low, the majority of patients having fewer than 10 seizures; 10–20% have just a single seizure. About 10–20% may have frequent seizures, but these also remit with age.

Children with Rolandic seizures may develop usually mild and reversible linguistic, cognitive and behavioural abnormalities during the active phase of the disease. These may be worse in children with onset of seizures before 8 years of age, high rate of occurrence and multifocal EEG spikes.

The development, social adaptation and occupations of adults with a previous history of Rolandic seizures were found normal.

Panayiotopoulos syndrome is remarkably benign in terms of its evolution. The risk of developing epilepsy in adult life is probably no more than of the general population. Most patients have one or 2-5 seizures. Only a third of patients may have more than 5 seizures, and these may be frequent, but outcome is again favorable. However, one fifth of patients may develop other types of infrequent, usually rolandic seizures during childhood and early teens. These are also age-related and remit before the age of 16 years. Atypical evolutions with absences and drop attacks are exceptional. Children with pre-existing neurobehavioral disorders tend to be pharmacoresistant and have frequent seizures though these also remit with age.

Formal neuropsychological assessment of children with Panayiotopoulos syndrome showed that these children have normal IQ and they are not on any significant risk of developing cognitive and behavioural aberrations, which when they occur they are usually mild and reversible. Prognosis of cognitive function is good even for patients with atypical evolutions.

However, though Panayiotopoulos syndrome is benign in terms of its evolution, autonomic seizures are potentially life-threatening in the rare context of cardiorespiratory arrest.

The mortality rate ranges from 3–7% in a mean follow up period of 8.5 to 9.7 years. Death is often related to accidents.

Panayiotopoulos syndrome probably affects 13% of children aged 3 to 6 years who have had 1 or more afebrile seizures and 6% of such children in the 1- to 15-year age group. All races and both sexes are affected.

Onset is between 3 and 15 years of age with a mean of around 8. Both sexes are equally affected. The disorder accounts for about 2–7% of benign childhood focal seizures.

Epilepsy with myoclonic-astatic seizures has a variable course and outcome. Spontaneous remission with normal development has been observed in a few untreated cases. Complete seizure control can be achieved in about half of the cases with antiepileptic drug treatment (Doose and Baier 1987b; Dulac et al. 1990). In the remainder of cases, the level of intelligence deteriorates and the children become severely intellectually disabled. Other neurologic abnormalities such as ataxia, poor motor function, dysarthria, and poor language development may emerge (Doose 1992b). However, this proportion may not be representative because in this series the data were collected in an institution for children with severe epilepsy.

The outcome is unfavorable if generalized tonic-clonic, tonic, or clonic seizures appear at the onset or occur frequently during the course. Generalized tonic-clonic seizures usually occur during the daytime in this disorder, at least in the early stages. Nocturnal generalized tonic-clonic seizures, which may develop later, are another unfavorable sign. If tonic seizures appear, prognosis is poor.

Status epilepticus with myoclonic, astatic, myoclonic-astatic, or absence seizures is another ominous sign, especially when prolonged or appearing early.

Failure to suppress the EEG abnormalities (4- to 7-Hz rhythms and spike-wave discharges) during therapy and absence of occipital alpha-rhythm with therapy also suggest a poor prognosis (Doose 1992a).

Jeavons syndrome is a lifelong disorder, even if seizures are well controlled with antiepileptic drugs. Men have a better prognosis than women. There is a tendency for photosensitivity to disappear in middle age, but eyelid myoclonia persists. It is highly resistant to treatment and occurs many times a day, often without apparent absences and even without demonstrable photosensitivity.

Childhood absence epilepsy is a fairly common disorder with a prevalence of 1 in 1000 people. Few of these people will likely have mutations in CACNA1H or GABRG2 as the prevalence of those in the studies presented is 10% or less.

The age of onset ranges from 1 to 14 years with 75% starting between 7–10 years. There is a 1.5 male predominance, prevalence is around 15% in children aged 1–15 years with non-febrile seizures and incidence is 10–20/100,000 of children aged 0–15 years

Generalized epilepsy, also known as primary generalized epilepsy or idiopathic epilepsy, is a form of epilepsy characterised by generalised seizures with no apparent cause. Generalized seizures, as opposed to focal seizures, are a type of seizure that impairs consciousness and distorts the electrical activity of the whole or a larger portion of the brain (which can be seen, for example, on electroencephalography, EEG).

Generalized epilepsy is "primary" because the epilepsy is the originally diagnosed condition itself, as opposed to "secondary" epilepsy, which occurs as a symptom of a diagnosed condition.

People with epilepsy are at an increased risk of death. This increase is between 1.6 and 4.1 fold greater than that of the general population and is often related to: the underlying cause of the seizures, status epilepticus, suicide, trauma, and sudden unexpected death in epilepsy (SUDEP). Death from status epilepticus is primarily due to an underlying problem rather than missing doses of medications. The risk of suicide is increased between two and six times in those with epilepsy. The cause of this is unclear. SUDEP appears to be partly related to the frequency of generalized tonic-clonic seizures and accounts for about 15% of epilepsy related deaths. It is unclear how to decrease its risk. The greatest increase in mortality from epilepsy is among the elderly. Those with epilepsy due to an unknown cause have little increased risk. In the United Kingdom, it is estimated that 40–60% of deaths are possibly preventable. In the developing world, many deaths are due to untreated epilepsy leading to falls or status epilepticus.

The prognosis of ICOE-G is unclear, although available data indicate that remission occurs in 50–60% of patients within 2–4 years of onset. Seizures show a dramatically good response to carbamazepine in more than 90% of patients. However, 40–50% of patients may continue to have visual seizures and infrequent secondarily generalized convulsions, particularly if they have not been appropriately treated with antiepileptic drugs.

LGS is seen in approximately 4% of children with epilepsy, and is more common in males than in females. Usual onset is between the ages of three and five. Children can have no neurological problems prior diagnosis, or have other forms of epilepsy. West syndrome is diagnosed in 20% of patients before it evolves into LGS at about 2 years old.

Seven anti-epileptic drugs are approved for use in cases of suspected primary generalized epilepsy:

- Felbamate

- Levetiracetam

- Zonisamide

- Topiramate

- Valproate

- Lamotrigine

- Perampanel

Valproate, a relatively old drug, is often considered the first-line treatment. It is highly effective, but its association with fetal malformations when taken in pregnancy limits its use in young women.

All anti-epileptic drugs (including the above) can be used in cases of partial seizures.

Benign familial infantile epilepsy (BFIE), also known as benign familial infantile seizures (BFIS) or benign familial infantile convulsions (BFIC) is an epilepsy syndrome. Affected children, who have no other health or developmental problems, develop seizures during infancy. These seizures have focal origin within the brain but may then spread to become generalised seizures. The seizures may occur several times a day, often grouped in clusters over one to three days followed by a gap of one to three months. Treatment with anticonvulsant drugs is not necessary but they are often prescribed and are effective at controlling the seizures. This form of epilepsy resolves after one or two years, and appears to be completely benign. The EEG of these children, between seizures, is normal. The brain appears normal on MRI scan.

A family history of epilepsy in infancy distinguishes this syndrome from the non-familial classification (see benign infantile epilepsy), though the latter may be simply sporadic cases of the same genetic mutations. The condition is inherited with an autosomal dominant transmission. There are several genes responsible for this syndrome, on chromosomes 2, 16 and 19. It is generally described as idiopathic, meaning that no other neurological condition is associated with it or causes it. However, there are some forms that are linked to neurological conditions. One variant known as infantile convulsions and choreoathetosis (ICCA) forms an association between BFIE and paroxysmal kinesigenic choreoathetosis and has been linked to the PRRT2 gene on chromosome 16. An association with some forms of familial hemiplegic migraine (FHM) has also been found. Benign familial infantile epilepsy is not genetically related to benign familial neonatal epilepsy (BFNE), which occurs in neonates. However, a variation with seizure onset between two days and seven months called "benign familial neonatal–infantile seizures" (BFNIS) has been described, which is due to a mutation in the SCN2A gene.

Gelastic seizures are usually not responsive to pharmacotherapy. They can produce secondary seizure characteristics which may respond to medications or surgery. These options are not a guaranteed cure, and depend primarily on the individual patient’s pathology.

The treatment depends on the cause of the seizures. If the seizures are caused by a tumor, surgical removal can be attempted. However, surgical removal is not always an immediate cure, and there can be complications. Complications can include cerebral infarcts, and cognitive deterioration. Hormonal treatment can be attempted to help individuals with precocious puberty. Anti-epileptic drugs could be an option as well depending on the patient’s criteria. These drugs could include carbamazepine, clobazam, lamotrigine, levetiracetam, oxcarbazepine and topiramate. However, usually none of these medications are capable of stopping the seizures from occurring, and like any medication, there may be undesirable side effects. There is also a specialized form of radiotherapy that may be an option depending on the tumor type and location. Once again, there are very few areas in the world that offer this treatment. Gamma knife radiosurgery can be the treatment of choice when it comes to hypothalamic hamartomas. It is a low risk option due to its lower frequency of neurological deficits. It is recommended for patients with tumors that don’t come into contact with the optic chiasm.

The most potent precipitating factor is eye closure, whether voluntary, involuntary or reflex. Most and, in some patients, all of the seizures are induced immediately after closure of the eyes in the presence of uninterrupted (non-flickering) light. Eye closure in total darkness is ineffective.

Contrary to other forms of photosensitive epilepsies that are sensitive only to flickering lights, patients with Jeavons syndrome are also sensitive to bright, non-flickering lights. This is probably due to the enhancing effect of bright light on the sensitivity of eye closure.

While many cases are not preventable, efforts to reduce head injuries, provide good care around the time of birth, and reduce environmental parasites such as the pork tapeworm may be effective. Efforts in one part of Central America to decrease rates of pork tapeworm resulted in a 50% decrease in new cases of epilepsy.

West syndrome is a triad of developmental delay, seizures termed infantile spasms, and EEG demonstrating a pattern termed hypsarrhythmia. Onset occurs between three months and two years, with peak onset between eight and 9 months. West syndrome may arise from idiopathic, symptomatic, or cryptogenic causes. The most common cause is tuberous sclerosis. The prognosis varies with the underlying cause. In general, most surviving patients remain with significant cognitive impairment and continuing seizures and may evolve to another eponymic syndrome, Lennox-Gastaut syndrome. It can be classified as idiopathic, syndromic, or cryptogenic depending on cause and can arise from both focal or generalized epileptic lesions.

Early myoclonic encephalopathy (EME) is an epilepsy syndrome where myoclonic seizures develop in the neonatal period. After several months, the seizure pattern may develop to infantile spasms (West syndrome). Various genetic and metabolic disorders are responsible. The seizures are resistant to treatment. The neurology is very abnormal and patients often do not live beyond one year.

Myoclonic astatic epilepsy, also known as myoclonic atonic epilepsy or Doose syndrome, is a generalized idiopathic epilepsy. It is characterized by the development of myoclonic seizures and/or myoclonic astatic seizures.